4 Neuromuscular Physiology: The Motor UnitLower Motor Neurons = Alpha Motor NeuronsAlpha Motor Neuron Cell BodiesCranial Musculature: In the BrainstemSomatic Cells: In the Anterior Horn of the Spinal CordNerve RootsPlexusPeripheral NervesTerminal RamificationsMotor Neuron SynapseLower motor neurons that conduct motor function signals are called “alpha motor neurons.” The cell bodies of alpha motor neurons are in 2 locations based on their target muscles. Alpha motor neurons that conduct signals to the cranial musculature have cell bodies that reside in the brainstem. Alpha motor neurons that conduct signals to the somatic cells are in the anterior horn of the spinal cord. Motor axons emerge through the dura, traveling from the brainstem or spinal cord, as nerve roots. The motor axons coalesce with other motor axons, sensory fibers, and autonomic fibers to form a plexus. The plexi then travel in peripheral nerves, coursing toward the muscles that they innervate. The alpha motor neurons are myelinated, resulting in increased speed of signal conduction. When the alpha motor neuron arrives at its target muscle, multiple terminal ramifications, or tiny branches, form many connections with the muscle, resulting in synapses on individual muscle fibers.palrehab.net/images/spin20.jpg

5 The Motor Unit Neuromuscular JunctionPresynaptic Acetylcholine ReleasePostsynaptic Acetylcholine BindingIncreases Muscle End-Plate PotentialThreshold Level > DepolarizesCalcium Ions Released from Sarcoplasmic ReticulumExcitation-Contraction Coupling > Muscle ContractionAcetylcholine Degraded by Cholinesteraseeducation.vetmed.vt.edu/Curriculum/VM8054/Labs/Lab10/IMAGES/MOTOR%20END%20PLATES%20SMALL%201.jpgThe alpha motor neuron communicates, or synapses, with muscle fiber at the neuromuscular junction. On the presynaptic side of the neuromuscular junction, acetylcholine is constructed, parceled, and stored for release. A signal then comes down from the brain, traveling through the alpha motor neuron in the anterior horn of the spinal cord, then through the axon to the target muscle. This signal causes depolarization of the presynaptic membrane, activating voltage-gated calcium channels. The acetylcholine packets are then draw to the presynaptic membrane, fuse with it, and then are expelled from it into the synaptic cleft. The acetylcholine migrates to the postsynaptic membrane, where they bind to receptors that cause an influx of sodium, resulting in an increased muscle endplate potential, and eventually causing muscle depolarization. Depolarization causes calcium ions to be released from the sarcoplasmic reticulum. Muscle contraction is a result of excitation-contraction coupling. The acetylcholine then gets degraded by cholinesterase. Choline is returned to the presynaptic membrane, where it is recycled.bp3.blogger.com/_v2GFIISzHOU/SAjilu3b8kI/AAAAAAAAASk/3BRF9vWKgYY/s400/Neuro-Muscular+Junction.jpg

7 Neuromuscular DisordersAcute Inflammatory Demyelinating Polyradiculoneuropathy (a.k.a. Guillain-Barre Syndrome)Motor >>Sensory Peripheral NeuropathyMonophasicNadir at 4 weeksImmune mediatedExact etiology unknownDemyelinating NeuropathyPrimary AxonopathyAcute Inflammatory Demyelinating Polyradiculoneuropathy is otherwise known as Guillain-Barre Syndrome. It is a peripheral neuropathy that affects motor nerves much more than sensory nerves. It has a monophasic course with nadir at approximately 4 weeks. The disease process appears to be immune mediated, with antibodies directed against components of the peripheral nerves. The exact etiology is still not clearly understood. Most patients undergo a demyelinating neuropathy. Approximately 5% suffer from a primary axonopathy.

8 Guillain-Barre Syndrome? Preceding disease or conditionGangliosidesCampylobacter jejuniMany different diseases and conditions have been implicated as the trigger for Guillain-Barre Syndrome. However, no single factor has been common to all cases of Guillain-Barre. There is however, a clear-cut link between the inflammatory response and the onset of Guillain-Barre. It is possible that antibodies are activated in response to the infection or condition and then the antibodies crossreact with peripheral nerve gangliosides. For example, antibodies against specific gangliosides have been identified following infection with Campylobacter jejuni.upload.wikimedia.org/wikipedia/commons/thumb/b/ba/Campylobacter.jpg/450px-Campylobacter.jpg

9 Guillain-Barre SyndromeClinical FindingsSubacuteProgressive weaknessStarts in legsSensory complaintsNo objective sensory deficitsDiminished or absent deep tendon reflexesMyelinClinical findings associated with Guillain-Barre Syndrome include a subacute onset of symptoms. The weakness begins in the legs and is progressive. Sensory complaints are often present with no findings consistent with sensory deficits. Deep tendon reflexes may slowly vanish after several days, so the patient may present with absent or diminished reflexes.upload.wikimedia.org/wikipedia/commons/c/c1/Myelinated_neuron.jpgdrdavis.typepad.com/.a/6a00d834525ed169e201156f86664c970c-320pi

10 Guillain-Barre SyndromeCSF findings, around 2nd weekElevated proteinNo pleocytosisThe diagnosis of Guillain-Barre is based primarily on disease course and clinical findings.CSF examination can be used to exclude other potential diagnoses. CSF findings usually start to appear around the second week and consist of elevated protein content without pleocytosis.neuromuscular.wustl.edu/pics/diagrams/emg/gbsrecov.gif

11 Guillain-Barre SyndromeElectrodiagnostic StudiesMotor and Sensory Nerve Conduction StudiesNeedle ElectromyographyFindings:Segmental nerve demyelinationMultifocal conduction blocksSlow Conduction VelocityConsistent with a Peripheral NeuropathyElectrodiagnostic studies, consisting of motor and sensory nerve conduction studies and Needle electromyography, can be used to substantiate the diagnosis of Guillain-Barre. The findings are consistent with segmental nerve demyelination, multifocal conduction block, and slow conduction velocities. These findings are consistent with a peripheral neuropathy.graphics8.nytimes.com/images/2007/08/01/health/adam/9238.jpg

12 Guillain-Barre SyndromeManagementVent supportAutonomic DysfunctionImmunotherapyPlasma exchangeHigh dose IVIgRehabilitationManagement of Guillain-Barre Syndrome is primarily supportive.-The patient should be monitored and if they progress to respiratory failure, should be intubated early. Full ventilatory support is often necessary for a week or more. Most patients are able to be extubated within 4 weeks.-Autonomic dysfunction often presents as a hypersympathetic state with unexplained sinus tachycardia. The patient may have hyperdynamic vital signs with bradycardia in response to vagal stimulation or viscus distention. Temporary pacing may be necessary. This is one of the major causes of death attributable to Guillain-Barre Syndrome-Immunotherapy is aimed at eliminating the antibodies directed against the peripheral nerves. Plasma exchange or high dose IVIG is often used to accomplish this. Both appear to be equivalent. Corticosteroids have not demonstrated a benefit in the treatment of Guillain-Barre Syndrome.repairstemcell.files.wordpress.com/2009/03/ms-pic.jpg

13 West Nile Virus West Nile Virus Acute Flaccid Paralysis SyndromeFlavivirusBirds and mosquitoes (Culex)Late summer or FallWest Nile Virus surfaced as a formidable neuromuscular disorder in 1999, during the outbreak in New York City. West Nile virus is a type of flavivirus. It is transmitted between birds and mosquitoes primarily. The Culex mosquito is responsible for the spread to humans. Clinical disease usually appears around late summer or fall. It is capable of being transmitted through blood.media.publicbroadcasting.net/kera/newsroom/images/ jpg

14 West Nile Virus 3 Different Clinical ManifestationsAsymptomatic infectionMild febrile syndrome West Nile Feverapprox. 20%3 – 6 days durationNeuroinvasive disease West Nile meningitis or encephalitisapprox. 1 in 150West Nile Virus has 3 distinct clinical manifestations: First, infection may be asymptomatic. Second, the infecton may be associated with a mild febrile syndrome, termed West Nile Fever. The is the case for approximately 20% of infected people. The syndrome typically lasts for 3 to 6 days. Third, approximately 1 in 150 with have neuroinvasive disease, termed West Nile meningitis or encephalitist2.gstatic.com/images?q=tbn:vSeOC3WZ2Wee0M:http://news.bbc.co.uk/nol/shared/spl/hi/health/03/travel_health/diseases/img/westnile.jpg

15 West Nile Virus Acute Flaccid Paralysis Syndrome “poliomyelitis-like”Ventral Horns and Ventral RootsAcuteAsymmetricalFlaccidNo Sensory DeficitsNo diffuse reflex deficitsNo bowel or bladder dysfunctionAcute Flaccid Paralysis Syndrome is a constellation of symptoms resulting in loss of neuromuscular function. The paralysis is similar to that which is seen with polio. The lesions are localized to the ventral horns or ventral roots. The paralysis is acute in onset and results in asymmetrical flaccid paralysis. Notably there is no evidence of sensory deficits, diffuse reflex deficits, or bowel or bladder dysfunction.

17 West Nile Virus – Acute Flaccid Paralysis SyndromeDiagnosisReverse-transcriptase PCR (insensitive)Antibody-capture ELISA (IgM)TreatmentSupportive?IVIg?Antiretroviral medicationsPrognosis for recovery of strength is poorWhen suspected, West Nile Virus associated Acute Flaccid Paralysis Syndrome can be confirmed by the findings of West Nile virus RNA in the patients serum, CSF, or other tissues, identified with reverse-transcriptase polymerase chain reaction. This test is however insensitive. An alternate and more sensitive test is the identification of West Nile virus IgM in the patient’s CSF or serum with the antibody-capture enzyme-linked immunosorbent assay.The treatment for acute flaccid paralysis is still largely supportive. Treatment with IV immunoglobulin and antiretroviral medications has been attempted without significant success. The prognosis for recovering strength is poor.

18 Myasthenia Gravis Autoimmune attack on acetylcholine receptorFluctuating weaknessProgressive with sustained exertionIncidence:Early adulthood:Women > MenLater adulthood:Women = MenMyasthenia gravis is another neuromuscular disease, caused by an autoimmune attack on the acetylcholine receptor of the postsynaptic membrane. Acetylcholine binding is blocked by the antibody. When the number of available receptors reaches 30%, the patient becomes symptomatic. This leads to fluctuating weakness that is worse after sustained exertion. Cardiac and smooth muscle are not affected. While the incidence is greater in young women than young men, the incidence becomes equal later in life

19 Myasthenia Gravis Clinical Presentation Muscle fatigueWorst with prolonged exertionOcular musclesPtosisDiplopiaBulbar musclesDysphagiaDysarthriaRespiratory FailureOcular muscles are frequently involved with myasthenia gravis leading to ptosis, as is seen here, and diplopia. The bulbar muscles are also often disturbed, leading to dysphagia and dysarthria. Along with these cranial nerve findings, respiratory failure is a common presenting symptom of myasthenia gravis.

21 Myasthenia Gravis Myasthenic Crisis 20% of patients with MGRespiratory failurePrecipitating factorsBronchopulmonary processesAspirationSepsisSurgical proceduresImmune modulation taperingCorticosteroidsPregnancyCertain DrugsNeuromuscular blocking agentsSensitive to Nondepolarizing agentsResistant to Depolarizing agentsThymomasMore fulminate disease30% of patients with myasthenic crisisMyasthenic crisis occurs in approximately 20% of patients with myasthenia gravis. These patients present with respiratory failure, requiring mechanical ventilation. There are many common precipitating factors including bronchopulmonary processes, aspiration, sepsis, surgical procedures, rapid immune modulation tapering, initiation of therapy with corticosteroids, preganancy, and certain drugs.Patients with myasthenia gravis are extremely sensitive to nondepolarizing neuromuscular blocking agents. They are resistant to Depolarizing neuromuscular blocking agents.Thymomas are a common finding in patients with myasthenia gravis. They are associated with a more fulminate disease course and are found in about 30% of patients with myasthenic crisis.

22 Myasthenia Gravis Treatment Immunomodulating MethodsPlasma exchange (short-term)Myasthenic crisisSurgical preparationIncreased strength after 2 to 3 exchangesIVIg (short-term)Alternative to plasma exchangePossible longer period until onset of effectCorticosteroidsOccasionally usedProlonged crisesTransient increase in weaknessOne of the components of treatment for myasthenia gravis is aimed at immunomodulation. Plasma exchange is an effective short-term treatment in most patients. It is employed for the treatment of myasthenic crisis and surgical preparation for MG patients. Strength begins to show a rise after approximately 2 to 3 exchanges.In patients who have a contraindication to plasma exchange such as poor vascular access or sepsis, IVIg can serve as an alternative. It’s an effective short-term treatment as well. The period of time until the onset of effect can be significantly longer.Corticosteroids are occasionally used for treatment of prolonged crises and crises refractory to the above treatments. If started early in the disease course, steroids can lead to a transient increase in weakness and may prolong the time that mechanical ventilation is required. This phenomenon has not been observed when steroids are started later in the hospitalization.

23 Myasthenia Gravis Treatment Cholinesterase inhibitorsCholinergic CrisisPossible increase in weaknessMuscle fasciculationsMuscarinic symptomsAvoid repeated/escalating dosesDiscontinue after intubationAcetylcholine ReceptorCholinesterase inhibitors are often used to attempt to ward off an impending myasthenic crisis. However, overzealous use can precipitate a cholinergic crisis. Signs of a cholinergic crisis include increased weakness, muscle fasciculations and symptoms associated with muscarinic symptoms such as miosis, lacrimation, salivation, abdominal cramping, nausea, vomiting, diarrhea, diaphoresis, and bradycardia.upload.wikimedia.org/wikipedia/commons/6/6e/Nicotinic_Acetylcholine_receptor.png

24 Myasthenia Gravis Thymus Abnormal in 75% Thymoma in 25% ThymectomyBenignMalignantThymectomyNecessary for thymomaControversial for patients without know thymic abnormalitiesDisease course often abatesMyasthenia gravis has a strong association with irregularities of the thymus. Up to 75% of patients have abnormal thymuses. Approximately 25% have thymomas, which may be benign or malignant.Thymectomy is therefore necessary in cases of thymoma. In patients who do not have known thymic abnormalities, the role for thymectomy is controversial. Following thymectomy, many patients experience cessation of symptoms.

25 Critical Illness Polyneuropathy & MyopathyGeneralized weaknessAxonalPredisposing FactorsCritical IllnessSepsisMultiple system organ failureProlonged mechanical ventilationCritical illness polyneuropathy and myopathy is the chief cause of new-onset generalized weakness in ICU patients who are not being treated for a primary neuromuscular disorder. This condition is primarily due to axonal pathology, as opposed to the demyelinating neuromuscular disorders such as Guillain-Barre Syndrome. Predisposing factors include critical illness, sepsis, and multiple system organ failure. It results in a need for mechanical ventilation for a prolonged period.

26 Critical Illness Polyneuropathy & MyopathyCommon AntecedentsSepsisMultiple System Organ FailurePathophysiologyICU daysNumber of invasive proceduresHyperglycemiaHypoalbuminemiaSeverity of MSOFNeuromuscular Blocking AgentsCorticosteroidsThe factors that lead to critical illness are not fully understood. Sepsis and multiple system organ failure are common to all patients who develop this disorder. Factors that correlate with disease are days spent in critical care, number of invasive procedures, hyperglycemia, hypoalbuminemia, severity of multiple system organ failure, neuromuscular blocking agents, and corticosteroids.

27 Critical Illness Polyneuropathy & MyopathyClinical FeaturesMuscle weakness and wastingParasthesiasDistal Sensory LossDeep Tendon ReflexesDiminished or absentClinical features include extremity muscle weakness and wasting, parasthesias, and distal sensory loss. Deep tendon reflexes may be diminished or absent. Few cases have been associated with facial or oropharyngeal weakness, differentiating from Guillain-Barre syndrome in which they are common.vasculitis.med.jhu.edu/typesof/images/Muscle_waste_MPA.jpg

29 Critical Illness Polyneuropathy & MyopathyPrognosisUnderlying critical illnessIncreased ventilator dependenceFunctional recovery in several monthsPadding and Positioning to prevent compression neuropathiesUlnar Nerve CompressionThe prognosis for patients suffering from critical illness polyneuropathy and myopathy is dependent on recovery from the underlying critical illness. This disorder results increased ventilator dependence with difficulty weaning. Nevertheless, most patients achieve full functional recovery within several months. During critical care and while the patient recovers from the generalized weakness and sensory deficits, stringent attention should be paid to padding and positioning to prevent compression neuropathies, which carry a worse prognosis.meddb.eznetpublish.ihealthspot.com/portals/2/MedicalLibraryAssets/Medical/CubitalTunnel_small.jpg

30 Compartment Syndrome Open or Closed Fractures Fixed CompartmentTissue edema and bleedingBlood flow impededCapillariesArteriolesFactors effecting tissue necrosisAmount of PressureDuration of increased pressureSensitivity of the tissue to ischemiaOne of the most common disorders of the muscular system frequently seen in the critical care is compartment syndrome. Compartment syndrome is often the result of trauma. It can occur with both open and closed fractures due to increased pressure within a fixed compartment. Following trauma, tissue edema and bleeding occur around the site of injury. If the pressure is too high, the capillaries and arterioles become compressed, unable to expand and deliver blood to the surrounding tissues. With compartment syndrome, the amount of tissue necrosis is dependent on several factors, including the amount of pressure in the compartment, the duration of the elevated pressure, and the sensitivity of that tissue to ischemia.Right Buttock Compartment Syndromecasesjournal.com/content/figures/ gif

31 Compartment Syndrome Tissue Ischemia Nervous tissue MuscleFunctional abnormalities after 30 minutesIrreversible damage after 12 to 24 hoursMuscleFunctional abnormalities after 2 to 4 hoursIrreversible damage after 4 to 12 hoursIncreased capillary permeability -> EdemaNecrotic MuscleTissues have different sensitivities and tolerance for ischemia. Nervous tissue is relatively tolerant with functional abnormalities developing after 30 minutes of ischemia but not progressing to irreversible damage until after 12 to 24. In contrast, muscle does not start to develop functional abnormalities until 2 to 4 hours after the onset of ischemia. However irreversible necrosis develops after only 4 to 12 hours of ischemia. As the compartment syndrome continues to progress and capillaries become more permeable, edema within the compartment continues to increase, accelerating the rate of tissue necrosis.

32 Compartment Syndrome Risk factors Severity of fractureExtent of soft tissue injuryCompressive devicesAnti-shock trousersTourniquetsSystemic hypotensionRisk factors that amplify the rate of tissue death include severity of the fracture and extent of soft tissue injury. The use of compressive devices to control hemorrhage, such as anti-shock trousers and tourniquets, cause tissue ischemia and subsequent reperfusion injury with a corresponding rise in tissue edema. The patient is therefore more likely have a compartment syndrome if these devices are used and correlating with their duration of use. The presence of systemic hypotension decreases muscle perfusion, as would be expected and subsequent compartment syndrome with tissue ischemia is more likely.

33 Compartment SyndromeMost common location = Anterior Compartment of the Lower Leg Usually from closed tibia fractureOther sitesThighArmButtockFootThe most common cause of acute compartment syndrome is traumatic injury with fractured bones. The most common site of acute compartment syndrome is the anterior compartment of the lower leg after closed tibia fractures. Other common sites of compartment syndrome are the thigh, arm, buttock, and foot.orthoinfo.aaos.org/figures/A00204F01.

34 Compartment Syndrome Diagnosis Clinical Tense compartment to palpationSevere pain with passive range of motionSevere compartment tendernessImpaired sensory examDecreased distal perfusionPulseless = Too LateExtensive tissue necrosis presentSerial Exams are CriticalThe diagnosis of compartment syndrome is clinical, based primarily on mechanism of injury, events following injury, symptoms and physical exam. On physical exam, the compartment is tense to palpation. The patient will have exquisite pain with passive range of motion and severe tenderness to palpation. The patient may have parasthesia and decreased sensation as the compartment syndrome progresses. As it becomes advanced, perfusion to the distal limb becomes compromised and may be mottled and cool with poor capillary refill. The limb will become pulseless if no intervention is taken. At this point, there is little chance of limb salvage as extensive tissue necrosis is present. Serial exams are critical in preventing the patient from reaching this stage by intervening before significant damage is done.

35 Compartment Syndrome Measurement of Compartment PressuresUnresponsive patientsPressure > 30 to 45 = Indication for FasciotomiesDiastolic BP – Compartment Pressure < 30 = indication for FasciotomiesCompartment pressures can be monitored in unresponsive patients who are unable to relay sensation using. If the compartment pressure is greater than 30, surgical treatment is warranted. Also, if the diastolic blood pressure minus the compartment pressure is less than 30, fasciotomies are warranted.35

36 Compartment Syndrome Treatment Surgical FasciotomiesFasciotomy within 12 hours = 68% normal functional resultHydrationMonitor electrolytesMonitor for infection of fasciotomy sitesIf compartment syndrome is diagnosed, the patient should undergo fasciotomies emergently to restore perfusion to the limb. Fasciotomies must be sufficient to allow for adequate decompression. If performed within 12 hours, there is a 68% chance that the patient will have a normal functional outcome. Hydration is important in order to prevent renal failure as a result of rhabdomyolysis. Also, due to the risk of rhabdomyolysis and renal failure, electrolytes should be monitored closely. The fasciotomy sites must be monitored for infection.upload.wikimedia.org/wikipedia/commons/d/da/Fasciotomy_leg.jpg

37 Lower Leg Fasciotomies2 incisions4 compartmentsAnterolateral IncisionAnterolateral IncisionThe most common site of compartment syndrome is the lower leg. The most reliable procedure for decompression is two-incision, four-compartment fasciotomies. The lateral incision is performed 1 to 2 cm anterior to the edge of the fibula. Extend the incision down through the skin and subcutaneous tissue. Use caution to avoid the minor saphenous vein and the peroneal nerve. Divide down to the fascia. Deep to this incision is the intermuscular septum that divides anterior and lateral compartments. The septum should be incised along the full length of the compartments in an “H” shape with transverse incisions at the two ends and a longitudinal incision between. The deep peroneal nerve should be located to ensure entry into both compartments.Anterolateral Incisionimg.medscape.com/pi/emed/ckb/orthopedic_surgery/ jpg

38 Lower Leg FasciotomiesMedial IncisionIncision 1 fingerbreadth posterior to medial edge of the tibiaLiberal LengthAvoid saphenous veinDivide fibers of soleus from tibiaNeurovascular bundlePosteriomedial IncisionPosteriomedial IncisionFor the medial incision, incise approx 1 fingerbreadth posterior to the medial edge of the tibia. A liberal incision should be made and carried down through the skin and subcutaneous tissue to the level of the fascia with careful attention to avoid the saphenous vein. In order to enter the deep posterior compartment, sharply and bluntly separate the muscle fibers of the soleus from the tibial edge. Identification of the neurovascular bundle ensures that the deep posterior compartment has been entered.img.medscape.com/pi/emed/ckb/orthopedic_surgery/ jpg

39 Upper Leg Fasciotomies3 CompartmentsAnteriorPosteriorMedialCompartment syndrome rare3 compartments blend with the hipLateral incision usually sufficientOccasionally requires medial incisionThe upper leg has 3 compartments: anterior, posterior, and medial. Compartment syndrome is rare because of the large volume required to increase interstitial pressure. Also, the 3 compartments blend with the hip, so blood is able to exit from the compartments. If a compartment syndrome is identified, a lateral incision is usually sufficient. Occasionally a medial incision may be necessary.

41 Foot Compartment Syndrome-Up to 10% of calcaneal fractures41% of crush injuries to the footNo classic sign of CSMost reliable sign: tense bulging tissueUp to 10% of patients presenting with calcaneal fractures may have a compartment syndrome. Up to 41% of crush injuries to the foot develop compartment syndrome. Unlike other compartments, there are no classic sign of CS in the foot. The most reliable sign appears to be tense bulging tissue.

42 Forearm and Hand FasciotomiesCompartment syndromes are less common than in the legSupracondylar humerus fx > antebrachial compartment syndromeAnterior compartment realeased with volar incisionDorsal incision if necessaryCompartment syndromes are less common in the upper extremities than in the legs. A supracondylar humerus fracture may lead to antebrachial compartment syndrome. A volar incision is made first to release the anterior compartment of the forearm including the carpal tunnel. A dorsal incision for posterior compartment decompression may be necessary.img.medscape.com/pi/emed/ckb/orthopedic_surgery/ jpgimg.medscape.com/pi/emed/ckb/orthopedic_surgery/ jpg

43 Hand Fasciotomies Compartment syndrome of the hands is rareThenar and Hypothenar Compartment FasciotomiesCompartment syndrome of the hands is rare? From TraumaMore often iatrogenic (A-line or IV infiltrate)10 Osseofascial CompartmentsCarpal tunnel release1 or 2 dorsal incisionsNo sensory nerve symptomsPressure > 20mmHg = CSjmedicalcasereports.com/content/figures/ gifDorsal Interosseus Compartment FasciotomiesCompartment syndrome of the hand is rare, infrequently occurring due to trauma and more often due to iatrogenic factors such as an A-line or IV infiltrate. There are 10 osseofascial compartment within the hand most of which can be released with a carpal tunnel release and 1 or 2 dorsal incisions.No sensory nerves run in the compartments and so patients with compartment syndrome have no sensory symptoms. Unlike other compartments, a pressure of 20mmHg is consistent with compartment syndrome and is an indication for fasciotomies.jmedicalcasereports.com/content/figures/ jpg

44 Rhabdomyolysis Damage to skeletal muscle Crush MetabolicInjures cellsDecreases perfusionMetabolicCell lysis due to edemaCalcium in sarcoplasmic reticulumMuscle contractionsDepletes ATPDamage to mitochondrionReactive oxygen speciesNeutrophils migrateIncreased inflammatory responseMuscle compresses local structures > Compartment Syndrome > Decreased PerfusionMuscle cells release potassium, phosphate, myoglobin, creatine kinase and uric acidRhabdomyolysis refers to the breakdown of muscle cells. It can be initiated by several different causes of muscle damage. Crush injuries damage the cells directly as well as impede perfusion. Metabolic etiologies may cause cell lysis. The inflammation due to muscle damage can further lead to cell lysis. Following cell lysis, calcium accumulates in the sarcomplasmic reticulum, causing repeated muscle contractions and depleting the cells ATP. In addition damage to the mitochondrion generates reactive oxygen species. Neutrophils migrate to the site of damage and increase the inflammatory response. The muscle as it swells compresses adjacent structures within the same compartment which results in a compartment syndrome. Perfusion is further decreased and muscle cells continue to die, releasing potassium, phosphate, myoglobin, creatine kinase and uric acid into the bloodstream.

45 Rhabdomyolysis Myoglobin Nephrotoxic Muscle swellingIntravascular volume deficitRenal hypoperfusionUric acidPrecipitates in renal tubulesAccumulates in renal tubulesRhabdomyolysis occurs when skeletal muscles are damaged and release myoglobin into the bloodstream. Myoglobin is an iron-containing pigment that can cause severe damage to the kidneys. The large mass of muscle tissue edema leads to depletion of intravascular fluid, compromising blood flow to the kidney. Uric acid precipitates in the tubules and may result in obstruction. Myoglobin accumulates in the renal tubules.

46 Rhabdomyolysis Myoglobinuria Plasma myoglobin > 1.5 mg/dLMyoglobin casts cause nephron obstructionUrine AcidificationTea-colored urineUrine dipstick + for bloodUrine – for red blood cells on microscopyMyoglobinuria occurs when the levels in plasma exceed 1.5 mg/dl. As the kidneys reabsorb more water, myoglobin casts form and obstruct the flow of fluid through the nephron. In addition , the high levels of uric acid causes acidification of the filtrate. Iron from the myoglobin generates reactive oxygen species, damaging the kidney cells. Acute tubular necrosis ensues. The kidney is rendered unable to perform filtration, electrolyte regulation, and hormone production (resulting in depletion of vitamin D and calcium).The myoglobinuria appears tea-colored. While urine dipstick appears postive for blood, microscopy reveals no red blood cells in the urine.lifeinthefastlane.com/wp-content/uploads/2009/12/image_34.jpg

47 Rhabdomyolysis Management Replete Volume Mannitol Sodium bicarbonateIncreases flushing of myoglobin from renal tubulesEffective radical scavengerSodium bicarbonateAlkalization of UrineDecreases cast formationDecreases direct toxic effect of myoglobin on the renal tubulesManagement of rhabdomyolysis is supportive and aimed at minimizing damage to the kidney. Volume repletion with maintainance of high urine ouput is the main goal of therapy. Mannitol has been shown in some trials to be effective, likely due to the increase in intravascular volume flushing myoglobin from the renal tubules. Mannitol is also an effective free radical scavenger, reducing damage to the nephron. Sodium bicarbonate has been used as a treatment to alkalinize urine, decreasing the deposition of myoglobin in the renal tubules, decreasing cast formation, and decreasing the toxic effects of myoglobin on the renal tubules.bioephemera.com/wp-content/uploads/2007/06/jimstanisg1.jpg

48 Myositis Ossificans Severe blunt trauma Intra-muscular hematomaDelayed ossification of the soft tissueSuspected to be due to premature return to strenuous activityMost common sites:- arms- quadriceps• Treatment- Conservative- Rarely, surgical debridementA rare event that may occur with severe blunt trauma to the muscle results in an intra-muscular hematoma that undergoes delayed ossification of the soft tissue. Newly formed bone may even form a marrow cavity. These most commonly occur in the arms or quadriceps. They are thought to be due to a premature return to strenuous activity. Treatment is primarily conservative. Symptomatic patients occassionally require surgical debridement of the abnormal tissue.